Investigation of cellular pathophysiological differences in ER stress and apoptosis formation between classical and atypical forms of ovine pulmonary adenocarcinomas

OPA is an infectious viral disease of sheep. JSRV, which causes the disease, is a slow virus and has oncogenic properties. There are two recognized forms of the disease, classical and atypical. These forms are very important in the prognosis and pathogenicity of the tumor. Although there are many diagnostic, prevalence and pathogenesis studies on the disease, these studies are not enough to explain the ER stress and apoptosis caused by the agent in cells. Therefore, in this study, we investigated the pathogenesis of ER stress and apoptosis in OPA-induced lung tissue. In addition, the differences of these findings between atypical and classical forms of the disease were also determined. For this purpose, 18 lung specimens were used in the study, which were detected by histopathologic, RT-PCR, immunohistochemical (IHC) and immunofluorescence (IF) methods. GRP78, ATF6, ATF4, CHOP, Bcl-2, BAX, and Caspase 3 in all 18 samples by IHC, IF, and Western Blot analysis methods. The atypical form exhibited elevated marker expression, accompanied by reduced Bcl-2 levels compared to the classical form. With these results, it was observed that apoptosis occurred in cells due to the formation of ER stress in OPA infections. In addition, it was determined that the atypical form of the disease caused ER stress more than the classical form and caused more severe apoptosis in cells.